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2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Define atherosclerosis.

A

A hardened plaque in the intima of an artery. It is an inflammatory process.

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2
Q

What can an atherosclerotic plaque cause?

A
  1. Heart attack.
  2. Stroke.
  3. Gangrene.
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3
Q

What are the constituents of an atheromatous plaque?

A
  1. Lipid core.
  2. Necrotic debris.
  3. Connective tissue.
  4. Fibrous cap.
  5. Lymphocytes.
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4
Q

Give 5 risk factors for atherosclerosis.

A
  1. Family history.
  2. Increasing age.
  3. Smoking.
  4. High levels of LDL’s.
  5. Obesity.
  6. Diabetes.
  7. Hypertension.
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5
Q

In which arteries would you be most likely to find atheromatous plaques?

A

In the peripheral and coronary arteries.

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6
Q

Which histological layer of the artery may be thinned by an atheromatous plaque?

A

The media.

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7
Q

What is the precursor for atherosclerosis.

A

Fatty streaks.

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8
Q

What can cause chemoattractant release?

A

A stimulus such as endothelial cell injury.

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9
Q

What are the functions of chemoattractants?

A

Chemoattractants signal to leukocytes. Leukocytes accumulate and migrate into vessel walls -> cytokine release e.g. IL-1, IL-6 -> inflammation!

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10
Q

Describe the process of leukocyte recruitment.

A
  1. Capture.
  2. Rolling.
  3. Slow rolling.
  4. Adhesion.
  5. Trans-migration.
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11
Q

Describe in 5 steps the progression of atherosclerosis.

A
  1. Fatty streaks.
  2. Intermediate lesions.
  3. Fibrous plaque.
  4. Plaque rupture.
  5. Plaque erosion.
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12
Q

Progression of atherosclerosis: what are the constituents of fatty streaks?

A

Foam cells and T-lymphocytes. Fatty streaks can develop in anyone from about 10 years old.

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13
Q

Progression of atherosclerosis: what are constituents of intermediate lesions?

A
  • Foam cells.
  • Smooth muscle cells.
  • T lymphocytes.
  • Platelet adhesion.
  • Extracellular lipid pools.
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14
Q

Progression of atherosclerosis: what are the constituents of fibrous plaques?

A
  • Fibrous cap overlies lipid core and necrotic debris.
  • Smooth muscle cells.
  • Macrophages.
  • Foam cells.
  • T lymphocytes.

Fibrous plaques can impede blood flow and are prone to rupture.

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15
Q

Progression of atherosclerosis: why might plaque rupture occur?

A

Fibrous plaques are constantly growing and receding. The fibrous cap has to be resorbed and redeposited in order to be maintained. If balance shifted in favour of inflammatory conditions, the cap becomes weak and the plaque ruptures. Thrombus formation and vessel occlusion.

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16
Q

What is the treatment for atherosclerosis?

A

Percutaneous coronary intervention (PCI).

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17
Q

What is the major limitation of PCI?

A

Restenosis.

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18
Q

How can restenosis be avoided following PCI?

A

Drug eluting stents: anti-proliferative and drugs that inhibit healing.

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19
Q

What is the key principle behind the pathogenesis of atherosclerosis?

A

It is an inflammatory process!

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20
Q

Define atherogenesis.

A

The development of an atherosclerotic plaque.

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21
Q

Define angina.

A

Angina is a type of IHD. It is a symptom of O2 supply/demand mismatch to the heart experienced on exertion.

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22
Q

What is the most common cause of angina?

A

Narrowing of the coronary arteries due to atherosclerosis.

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23
Q

Give 5 possible causes of angina.

A
  1. Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis.
  2. Increased distal resistance = LV hypertrophy.
  3. Reduced O2 carrying capacity e.g. anaemia.
  4. Coronary artery spasm.
  5. Thrombosis.
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24
Q

Give 5 modifiable risk factors for angina.

A
  1. Smoking.
  2. Diabetes.
  3. High cholesterol (LDL).
  4. Obesity/sedentary lifestyle.
  5. Hypertension.
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25
Q

Give 3 non-modifiable risk factors for angina.

A
  1. Increasing age.
  2. Gender, male bias.
  3. Family history/genetics.
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26
Q

Briefly describe the pathophysiology of angina that results from atherosclerosis.

A

On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.

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27
Q

Briefly describe the pathophysiology of angina that results from anaemia.

A

On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -> myocardial ischaemia -> angina.

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28
Q

How do blood vessels try and compensate for increased myocardial demand during exercise.

A

When myocardial demand increases e.g. during exercise, microvascular resistance drops and flow increases!

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29
Q

Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?

A

In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can’t drop anymore and flow can’t increase to meet metabolic demand = angina!

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30
Q

How can angina be reversed?

A

Resting - reducing myocardial demand.

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31
Q

How would you describe the chest pain in angina?

A

Crushing central chest pain. Heavy and tight. The patient will often make a fist shape to describe the pain.

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32
Q

Give 5 symptoms of angina.

A
  1. Crushing central chest pain.
  2. The pain is relieved with rest or using a GTN spray.
  3. The pain is provoked by physical exertion.
  4. The pain might radiate to the arms, neck or jaw.
  5. Breathlessness.
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33
Q

What tool can you use to determine the best investigations and treatment in someone you suspect to have angina?

A

Pre-test probability of CAD. It takes into account gender, age and typicality of pain.

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34
Q

What investigations might you do in someone you suspect to have stable angina?

A
  1. ECG - usually normal
  2. CT angiography - inject contrast, can see narrowing
  3. HbA1c (for diabetes)
  4. FBC (check for anaemia)
  5. U+E (before starting ACEI)
  6. LFT (before starting statins)
  7. TFT (look for hyper/hypothyroidism)
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35
Q

A young, healthy, female patient presents to you with what appears to be the signs and symptoms of angina. Would it be good to do CT angiography on this patient?

A

Yes. CT angiography has a high NPV and so is ideal for excluding CAD in
younger, low risk individuals.

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36
Q

Describe the primary prevention of angina.

A
  1. Risk factor modification.

2. Low dose aspirin.

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37
Q

Describe the secondary prevention of angina.

A
  1. Risk factor modification.
  2. Pharmacological therapies for symptom relief and to reduce the risk of CV events (4As)
  3. Interventional therapies e.g. PCI.
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38
Q

Name 3 symptom relieving pharmacological therapies (long term symptomatic relief) that might be used in someone with angina.

A
  1. Beta blockers (bisoprolol)
  2. Nitrates e.g. GTN spray.
  3. Calcium channel blockers (amlodipine)
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39
Q

Describe the action of beta blockers.

A

Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. Myocardial work is reduced and so is myocardial demand = symptom relief.

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40
Q

Give 3 side effects of beta blockers.

A
  1. Bradycardia.
  2. Tiredness.
  3. Erectile dysfunction.
  4. Cold peripheries.
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41
Q

When might beta blockers be contraindicated?

A

They might be contraindicated in someone with asthma or in someone who is bradycardic.

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42
Q

Describe the action of nitrates.

A

Nitrates e.g. GTN spray are venodilators. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.

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43
Q

Describe the action of Ca2+ channel blockers.

A

Ca2+ blockers are arterodilators -> reduced BP -> reduced afterload -> reduced myocardial demand.

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44
Q

Name drugs used for angina secondary prevention

A

4As

  1. Antiplatelets (dual: aspirin + clopidogrel)
  2. Atorvastatin
  3. ACEI (ramipril)
  4. Atenolol (BB)
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45
Q

How does aspirin work?

A

Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Caution: Gastric ulcers!

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46
Q

What are statins used for?

A

They reduce the amount of LDL in the blood.

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47
Q

What is revascularisation?

A

Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.

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48
Q

Name 2 types of revascularisation.

A
  1. PCI.

2. CABG.

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49
Q

Give 2 advantages and 1 disadvantage of PCI.

A
  1. Less invasive.
  2. Convenient and acceptable.
  3. High risk of restenosis.
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50
Q

Give 1 advantage and 2 disadvantages of CABG.

A
  1. Good prognosis after surgery.
  2. Very invasive.
  3. Long recovery time.
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51
Q

What are acute coronary syndromes (ACS)?

A

ACS encompasses a spectrum of acute cardiac conditions including unstable angina, NSTEMI and STEMI.

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52
Q

What is the common cause of ACS?

A

Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.

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53
Q

What are uncommon causes of ACS?

A
  1. Coronary vasospasm.
  2. Drug abuse.
  3. Coronary artery dissection.
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54
Q

Briefly describe the pathophysiology of ACS?

A

Atherosclerosis -> plaque rupture -> platelet aggregation -> thrombosis formation -> ischaemia and infarction -> necrosis of cells -> permanent heart muscle damage and ACS.

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55
Q

Describe type 1 MI.

A

Spontaneous MI with ischaemia due to plaque rupture.

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56
Q

Describe type 2 MI.

A

MI secondary to ischaemia due to increased O2 demand.

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57
Q

Why do you see increased serum troponin in NSTEMI and STEMI?

A

The occluding thrombus causes necrosis of cells and so myocardial damage. Troponin is a sensitive marker for cardiac muscle injury and so is significantly raised in reflection to this.

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58
Q

Give 3 signs of unstable angina. troponin ?

A
  1. Cardiac chest pain at rest.
  2. Cardiac chest pain with crescendo patterns; pain becomes more frequent and easier provoked.
  3. No significant rise in troponin.
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59
Q

Give 6 signs/symptoms of MI.

A
  1. Unremitting and usually severe central cardiac chest pain.
  2. Pain occurs at rest.
  3. Sweating
  4. Breathlessness.
  5. Nausea/vomiting.
  6. 1/3 occur in bed at night.
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60
Q

Give 5 potential complications of MI.

A
  1. Heart failure.
  2. Rupture of infarcted ventricle.
  3. Rupture of interventricular septum.
  4. Mitral regurgitation.
  5. Arrhythmias.
  6. Heart block.
  7. Pericarditis.
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61
Q

What investigations would you do on someone you suspect to have ACS?

A
  1. ECG.
  2. Blood tests; look at serum troponin! FBC (anaemia), U+E (prior to ACEI), LFT (prior to statin), lipid profile, TFT, HbA1c (for diabetes)
  3. Coronary angiography.
  4. Echo (monitoring for arrhythmias)
  5. CXR (investigate causes)
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62
Q

What might the ECG of someone with unstable angina show?

A

The ECG from someone with unstable angina may be normal or might show T wave inversion and ST depression.

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63
Q

What might the ECG of someone with NSTEMI show?

A

The ECG from someone with NSTEMI may be normal or might show T wave inversion and ST depression. There also might be R wave regression, ST elevation and biphasic T wave in lead V3. pathological Q waves

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64
Q

What might the ECG of someone with STEMI show?

A

The ECG from someone with STEMI will show ST elevation in the anterolateral leads. After a few hours, T waves invert and deep, broad, pathological Q waves develop.

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65
Q

What would the serum troponin level be like in someone with unstable angina?

A

Normal.

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66
Q

What would the serum troponin level be like in someone with NSTEMI/STEMI?

A

Significantly raised.

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67
Q

A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?

A
  1. Gram negative sepsis.
  2. Pulmonary embolism.
  3. Myocarditis.
  4. Heart failure.
  5. Arrhythmias.
  6. pericarditis
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68
Q

Describe the initial management for ACS.

A
  1. Get into hospital ASAP - call 999.
  2. Aspirin 300mg.
  3. ECG: If STEMI, paramedics should call PCI centre for transfer.
  4. Pain relief e.g. morphine.
  5. Oxygen if hypoxic.
  6. Nitrates.

MONA

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69
Q

What is the treatment of choice for STEMI?

A
  • 300mg loading dose aspirin (anyone suspected with ACS)
  • PCI (within 2 hours)
  • Thrombolysis - streptokinase (If PCI not available within 2 hours or contraindicated)
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70
Q

What is the function of P2Y12?

A

It amplifies platelet activation.

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71
Q

Give 3 potential side effects of P2Y12 inhibitors.

A
  1. Bleeding.
  2. Rash.
  3. GI disturbances.
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72
Q

Describe the secondary prevention therapy for people after having a STEMI.

A

6As

  1. Aspirin.
  2. Another anti platelet - Clopidogrel (P2Y12 inhibitor).
  3. atorvastatin
  4. Atenolol (beta blocker).
  5. ACE inhibitor (ramipril).
  6. Aldosterone antagonist (if clinical HF)
  7. Modification of risk factors and cardiac rehab
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73
Q

ECG: what is the J point?

A

Where the QRS complex becomes the ST segment.

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74
Q

ECG: what is the normal axis of the QRS complex?

A

-30° -> +90°

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75
Q

ECG: what does the P wave represent?

A

Atrial depolarisation.

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76
Q

ECG: how long should the PR interval be?

A

120 - 200ms.

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77
Q

ECG: what might a long PR interval indicate?

A

Heart block.

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78
Q

ECG: how long should the QT interval be?

A

0.35 - 0.45s.

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79
Q

ECG: what does the QRS complex represent?

A

Ventricular depolarisation.

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80
Q

ECG: what does the T wave represent?

A

Ventricular repolarisation.

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81
Q

ECG: where would you place lead 1?

A

From the right arm to the left arm with the positive electrode being at the left arm. At 0°.

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82
Q

ECG: where would you place lead 2?

A

From the right arm to the left leg with the positive electrode being at the left leg. At 60°.

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83
Q

ECG: where would you place lead 3?

A

From the left arm to the left leg with the positive electrode being at the left leg. At 120°.

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84
Q

ECG: where would you place lead avF?

A

From halfway between the left arm and right arm to the left leg with the positive electrode being at the left leg. At 90°.

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85
Q

ECG: where would you place lead avL?

A

From halfway between the right arm and left leg to the left arm with the positive electrode being at the left arm. At -30°.

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86
Q

ECG: where would you place lead avR?

A

From halfway between the left arm and left leg to the right arm with the positive electrode being at the right arm. At -150°.

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87
Q

What is the dominant pacemaker of the heart?

A

The SA node. 60-100 beats/min.

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88
Q

How many seconds do the following represent on ECG paper?

a) small squares.
b) large squares.

A

a) 0.04s.

b) 0.2s.

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89
Q

How long should the QRS complex be?

A

Less than 110 ms.

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90
Q

In which leads would you expect the QRS complex to be upright in?

A

Leads 1 and 2.

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91
Q

In which lead are all waves negative?

A

aVR.

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92
Q

In which leads must the R wave grow?

A

From chest leads V1 to V4.

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93
Q

In which leads must the S wave grow?

A

From chest leads V1 to V3. It must also disappear in V6.

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94
Q

In which leads should T waves and P waves be upright?

A

Leads 1, 2, V2 -> V6.

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95
Q

What might tall pointed P waves on an ECG suggest?

A

Right atrial enlargement.

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96
Q

What might notched, ‘m shaped’ P waves on an ECG suggest?

A

Left atrial enlargement.

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97
Q

Give 3 signs of abnormal T waves.

A
  1. Symmetrical.
  2. Tall and peaked.
  3. Biphasic or inverted.
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98
Q

What happens to the QT interval when HR increases?

A

The QT interval decreases.

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99
Q

What part of the ECG does the plateau phase of the cardiac action potential coincide with?

A

QT interval.

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100
Q

What are the symptoms of DVT?

A

Non-specific symptoms, pain and swelling. Tenderness, warmth and slight discolouration.

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101
Q

Briefly describe the investigations might be done in order to diagnose a DVT.

A
  1. D-dimer; looks for fibrin breakdown products. If normal, you can exclude DVT. Abnormal does not confirm diagnosis however.
  2. Ultrasound compression scan; if you can’t squash the vein = clot.
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102
Q

What is the treatment for DVT?

A
  1. DOAC (apixaban)
  2. Or LMWH or warfarin.
  3. Compression stockings.
  4. Treat the underlying cause e.g. malignancy or thrombophilia.
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103
Q

Give 5 risk factors for DVT.

A
  1. Surgery, immobility, leg fracture.
  2. OCP, HRT.
  3. Long haul flights.
  4. Genetic predisposition.
  5. Pregnancy.
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104
Q

How can DVT’s be prevented?

A
  1. Hydration.
  2. Mobilisation.
  3. Compression stockings.
  4. Low does LMWH.
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105
Q

What might be the consequence of a dislodged DVT?

A

Pulmonary embolism.

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106
Q

How would you describe an arterial thrombosis?

A

Platelet rich - a ‘white thrombosis’.

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107
Q

How would you describe a venous thrombosis?

A

Fibrin rich - a ‘red thrombosis’.

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108
Q

What are the potential consequences of arterial thrombosis?

A
  1. MI.
  2. Stroke.
  3. Peripheral vascular disease e.g. gangrene
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109
Q

What are the potential consequences of venous thrombosis?

A

Pulmonary embolism.

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110
Q

What is the treatment for arterial thrombosis?

A
  1. Aspirin.
  2. LMWH.
  3. Thrombolytic therapy (streptokinase)
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111
Q

How does warfarin work?

A

It produces NON-functional clotting factors 2, 7, 9 and 10.

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112
Q

What is warfarin the antagonist of?

A

Vitamin K.

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113
Q

Why is warfarin difficult to use?

A
  1. Lots of interactions!
  2. Teratogenic.
  3. Needs almost constant monitoring.
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114
Q

What is infective endocarditis?

A

Infection of the heart valves.

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115
Q

What is the clinical diagnosis of hypertension?

A

BP ≥ 140/90mmHg.

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116
Q

How can hypertension be treated?

A
  1. Lifestyle modification e.g. reduce salt intake.

2. Anti-hypertensive drugs.

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117
Q

Write an equation for BP.

A

BP = CO X TPR.

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118
Q

Name 2 systems that are targeted pharmacologically in the treatment of hypertension.

A
  1. RAAS.

2. Sympathetic nervous system (NAd).

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119
Q

Give 4 functions of angiotensin 2.

A
  1. Potent vasoconstrictor.
  2. Activates sympathetic nervous system; increased NAd.
  3. Activates aldosterone = Na+ retention.
  4. Vascular growth, hyperplasia and hypertrophy.
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120
Q

Give 3 ways in which the sympathetic nervous system (NAd) lead to increased BP.

A
  1. Noradrenaline is a vasoconstrictor = increased TPR.
  2. NAd has positive chronotropic and inotropic effects.
  3. It can cause increased renin release.
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121
Q

Name 3 ACE inhibitors.

A
  1. Ramapril.
  2. Enalapril.
  3. Perindopril.
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122
Q

In what diseases are ACE inhibitors clinically indicated?

A
  1. Hypertension.
  2. Heart failure.
  3. Diabetic nephropathy.
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123
Q

Give 4 potential side effects of ACE inhibitors.

A

(related to decreased AII)

  1. Hypotension.
  2. Hyperkalaemia.
  3. Acute renal failure.
  4. Teratogenic.

(related to increased kinin)
5. dry chronic cough

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124
Q

Why do ACE inhibitors lead to increased kinin production?

A

ACE also converts bradykinin to inactive peptides. Therefore ACE inhibitors lead to a build up of kinin.

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125
Q

ACE inhibitors: give 3 potential side effects that are due to increased kinin production.

A
  1. Dry chronic cough.
  2. Rash.
  3. Anaphylactoid reaction.
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126
Q

You see a patient who is taking ramipril. They say that since starting the medication they have had a dry and persistent cough. What might have caused this?

A

ACE inhibitors lead to a build up of kinin. One of the side effects of this is a dry and chronic cough.

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127
Q

What are ARBs?

A

Angiotensin 2 receptor blockers.

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128
Q

At which receptor do ARB’s work?

A

AT-1 receptor.

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129
Q

Name 3 ARBs?

A
  1. Candesartan.
  2. Valsartan.
  3. Losartan.
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130
Q

In what diseases are ARBs clinically indicated?

A
  1. Hypertension.
  2. Heart failure.
  3. Diabetic nephropathy.
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131
Q

A patient with hypertension has come to see you about their medication. You see in their notes that ACE inhibitors are contraindicated. What might you prescribe them instead?

A

An ARB e.g. candesartan.

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132
Q

Give 4 potential side effects of ARBs.

A

ARBs have similar side effects to ACEi:

  1. Hypotension.
  2. Hyperkalaemia.
  3. Renal dysfunction.
  4. Rash.

Contraindicated in pregnancy.

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133
Q

Name 4 Calcium channel blockers.

A
  1. Amlodipine.
  2. Felodipine.
  3. Diltiazem.
  4. Verapamil.
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134
Q

Name 2 dihydropyridines and briefly explain how they work.

A

Dihydropyridines are a class of calcium channel blockers. Amlodipine and felodipine are examples of dihydropyridines. They are arterial vasodilators.

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135
Q

Name a calcium channel blocker that acts primarily on the heart.

A

Verapamil - it is negatively chronotropic and inotropic.

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136
Q

Name a calcium channel blocker that acts on the heart and on blood vessels.

A

Diltiazem - acts on the heart and the vasculature.

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137
Q

In what diseases are calcium channel blockers clinically indicated?

A
  1. Hypertension.
  2. IHD.
  3. Arrhythmia.
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138
Q

On what channels do calcium channel blockers work?

A

L type Ca2+ channels.

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139
Q

Give 3 potential side effects that are due to the vasodilatory ability of calcium channel blockers.

A
  1. Flushing.
  2. Headache.
  3. Oedema.
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140
Q

Give a potential side effect that is due to the negatively inotropic ability of calcium channel blockers.

A

Worsening caridac failure.

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141
Q

Give 2 potential side effects that are due to the negatively chronotropic ability of calcium channel blockers.

A
  1. Bradycardia.

2. Atrioventricular block.

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142
Q

Give 4 potential side effects of verapamil.

A
  1. Worsening cardiac failure (-ve inotrope).
  2. Bradycardia (-ve chronotrope).
  3. Atrioventricular block (-ve chronotrope).
  4. Constipation!
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143
Q

A patient comes to see you who has recently started taking calcium channel blockers for their hypertension. They complain of constipation. What calcium channel blocker might they be taking?

A

Verapamil.

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144
Q

Name 3 beta blockers.

A
  1. Bisoprolol (beta 1 selective).
  2. Atenolol.
  3. Propanolol (beta 1/2 non selective).
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145
Q

In what diseases are beta blockers clinically indicated?

A
  1. IHD.
  2. Heart failure.
  3. Arrhythmia.
  4. Hypertension.
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146
Q

Give 5 potential side effects of beta blockers.

A
  1. Fatigue.
  2. Headache.
  3. Nightmares.
  4. Bradycardia.
  5. Hypotension.
  6. Cold peripheries.
  7. Erectile dysfunction.
  8. Bronchospasm.
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147
Q

Diuretics: where do in the kidney do thiazides work?

A

The distal tubule.

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148
Q

Name a thiazide.

A

Bendroflumethiazide.

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149
Q

Name 2 loop diuretics.

A
  1. Furosemide.

2. Bumetanide.

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150
Q

Name a potassium sparing diuretic.

A

Spironolactone.

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151
Q

Why are potassium sparing diuretics especially effective?

A

They have anti-aldosterone effects too.

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152
Q

In what diseases are diuretics clinically indicated?

A
  1. Heart failure.

2. Hypertension.

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153
Q

Give 5 potential side effects of diuretics.

A
  1. Hypovolemia.
  2. Hypotension.
  3. Reduced serum Na+/K+/Mg+/Ca2+.
  4. Increased uric acid -> gout.
  5. Erectile dysfunction.
  6. Impaired glucose tolerance.
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154
Q

You see a 45 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?

A

ACE inhibitors e.g. ramapril or ARB e.g. candesartan.

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155
Q

You see a 65 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?

A

Calcium channel blockers (as this patient is over 55) e.g. amlodipine.

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156
Q

You see a 45 y/o patient who has recently started taking ACE inhibitors for their hypertension. Unfortunately their hypertension still isn’t controlled. What would you do next for this patient?

A

You would combine ACE inhibitors or ARB with calcium channel blockers.

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157
Q

You see a 45 y/o patient who has been taking ACE inhibitors and calcium channel blockers for their hypertension. Following several tests you notice that their blood pressure is still high. What would you do next for this patient?

A

You would combine the ACEi/ARB and calcium channel blockers with a thiazide diuretic e.g. bendroflumethiazide.

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158
Q

What is heart failure?

A

a syndrome in which patients have symptoms and signs resulting from an abnormality of cardiac structure and/or function

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159
Q

What is the most common cause (4) of heart failure?

A

Ischaemic heart disease.

hypertension
aortic stenosis
arrhythmias

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160
Q

What might you give to someone with hypertension if they are ACE inhibitor intolerant?

A

ARB (candesartan).

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161
Q

What hormones does the heart produce?

A

ANP and BNP.

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162
Q

What metabolises ANP and BNP?

A

NEP.

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163
Q

Why can NEP inhibitors work for heart failure treatment?

A

NEP metabolises ANP and BNP. NEP inhibitors can therefore increase levels of ANP and BNP in the serum.

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164
Q

What are the functions of ANP and BNP?

A
  1. Increased renal excretion of Na+ and therefore water.
  2. Vasodilators.
  3. Inhibit aldosterone release.
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165
Q

What is the counter regulatory system to RAAS?

A

ANP/BNP hormones.

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166
Q

Name 2 nitrates that are used pharmacologically.

A
  1. Isosorbide mononitrate.

2. GTN spray.

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167
Q

How do nitrates work in the treatment of heart failure?

A

They are venodilators. They reduce preload and so BP.

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168
Q

Give 3 potential side effects of nitrates.

A
  1. Headache, dizzy, lightheadedness
  2. Syncope.
  3. Tolerance.
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169
Q

What classification is used to group anti-arrhythmic drugs?

A

Vaughan Williams classification.

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170
Q

Vaughan Williams classification: name 3 class 1 drugs.

A

Class 1 are Na+ channel blockers. There are 3 sub-divisions in this group.

1a: disopyramide.
1b: lidocaine.
1c: flecainide.

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171
Q

Vaughan Williams classification: name 3 class 2 drugs.

A

Class 2 are beta blockers:

  1. Propranolol.
  2. Atenolol.
  3. Bisoprolol.
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172
Q

Vaughan Williams classification: name a class 3 drug.

A

Class 3 drugs prolong the action potential. E.g. amiodarone. Side effects are very likely with these drugs.

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173
Q

Vaughan Williams classification: name 2 class 4 drugs.

A

Class 4 drugs are calcium channel blockers but NOT dihydropyridines as these don’t effect the heart.

  1. Verapamil.
  2. Diltiazem.
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174
Q

How does digoxin work?

A

It inhibits the Na+/K+ pump therefore making the action potential more positive and ACh is released from parasympathetic nerves.

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175
Q

What are the main effects of digoxin?

A
  1. Bradycardia (negative chronotrope)
  2. Reduced atrioventricular conduction.
  3. Increased force of contraction (positive inotrope).
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176
Q

Give 4 potential side effects of digoxin.

A
  1. Nausea.
  2. Vomiting.
  3. Diarrhoea.
  4. Confusion.
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177
Q

In what diseases is digoxin clinically indicated?

A

Atrial fibrillation and severe heart failure.

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178
Q

Name 2 drugs that can prolong the QT interval.

A
  1. Sotalol.

2. Amiodarone.

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179
Q

Give 5 potential side effects of drugs that prolong the QT interval.

A
  1. Pro-arrythmic effects.
  2. Interstitial pneumonitis.
  3. Abnormal liver function.
  4. Hyper/hypothyroidism.
  5. Sun sensitivity.
  6. Grey skin discolouration.
  7. Corneal micro-deposits.
  8. Optic neuropathy.
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180
Q

How do sodium channel blockers work in the treatment of ventricular tachycardia?

A

They block the inactivation gate of the sodium channel.

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181
Q

What additional property makes propranolol the most useful beta blocker to help control the arrhythmias which occur immediately following a heart attack ?

A

It can also block sodium channels.

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182
Q

What does furosemide block?

A

The Na+/K+/2Cl- transporter.

its an antihypertensive drug

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183
Q

Why are beta blockers good in chronic heart failure?

A

They block reflex sympathetic responses which stress the failing heart.

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184
Q

Doxazosin can be used in the treatment of hypertension. How does this drug work?

A

It is an alpha 1 receptor antagonist.

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185
Q

How do beta blockers provide symptom relief in angina?

A
  1. They reduce O2 demand by slowing heart rate (negative chronotrope).
  2. They reduce O2 demand by reducing myocardial contractility (negative inotrope).
  3. They increase O2 distribution by slowing heart rate.
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186
Q

What drug might you give to someone with angina caused by coronary artery vasospasm?

A

Amlodipine.

187
Q

Define shock.

A

When the cardiovascular system is unable to provide adequate substrate for aerobic cellular respiration.

188
Q

Give 7 signs/symptoms of shock.

A
  1. Pale.
  2. Sweaty.
  3. Cold.
  4. Pulse is weak and rapid.
  5. Reduced urine output.
  6. Confusion.
  7. reduced consciousness
  8. low oxygen sats
189
Q

What can cause hypovolemic shock?

A
  1. Loss of blood e.g. acute GI bleeding, trauma, post-op, splenic rupture.
  2. Loss of fluid e.g. dehydration, burns, vomiting, pancreatitis.
190
Q

What can cause cardiogenic shock?

A
  1. Cardiac tamponade.
  2. Pulmonary embolism.
  3. Acute MI.
  4. Fluid overload.
191
Q

What is septic shock?

A

A systemic inflammatory response associated with an infection (bacterial endotoxins).

192
Q

What is anaphylactic shock?

A

A severe type 1 hypersensitivity reaction associated with massive histamine release (mast cell degranulation) = haemodynamic collapse. The patient may be breathless, wheezy and have a rash.

193
Q

What is the treatment for anaphylactic shock?

how can you confirm diagnosis after

A

Airway (patent)
Breathing (oxygen if required, salbutamol)
Circulation (IV fluid bolus)
Disability (Lie patient flat -> increase cerebral perfusion)
Exposure (remove trigger)
once diagnosed: IM adrenaline, oral antihistamines, IV steroids (hydrocortisone)
confirm diagnosis: elevated tryptase (with 6 hrs)

194
Q

Give 2 signs of ARDS.

A
  1. Impaired oxygenation.
  2. Bilateral pulmonary infiltrates.
  3. No cardiac failure.
195
Q

Describe the pathophysiology of ARDS in 3 stages.

A
  1. Exudative phase: increased vascular permeability leads to a platelet, fibrin and clotting factor rich exudate.
  2. Proliferative phase: fibroblast proliferation.
  3. Fibrotic phase.
196
Q

Give 4 extra-pulmonary causes of ARDS.

A
  1. SEPSIS!
  2. Trauma.
  3. Shock.
  4. Drug reaction.
  5. Pancreatitis.
197
Q

Give 3 pulmonary causes of ARDS.

A
  1. Pneumonia.
  2. Smoke inhalation.
  3. Near drowning.
198
Q

How much serous fluid is there between the visceral and parietal pericardium?

A

50ml.

199
Q

What is the function of the serous fluid between the visceral and parietal pericardium?

A

It acts as a lubricant and so allows smooth movement of the heart inside the pericardium.

200
Q

What is the function of pericardium?

A

It restrains the filling volume of the heart.

201
Q

Describe the aetiology of pericarditis.

A
  1. Viral (common) e.g. enteroviruses.
  2. Bacterial e.g. mycobacterium tuberculosis.
  3. Autoimmune e.g. RA, sjögren syndrome.
  4. Neoplastic.
  5. Metabolic e.g. uraemia.
  6. Traumatic and iatrogenic.
  7. 80-90% are idiopathic.
202
Q

What is acute pericarditis?

A

An inflammatory pericardial syndrome with or without effusion.

203
Q

How can acute pericarditis be clinically diagnosed?

A

Acute pericarditis can be clinically diagnosed if the patient has at least 2 of the following:

  1. Chest pain.
  2. Friction rub.
  3. ECG changes.
  4. Pericardial effusion.
204
Q

Give 5 symptoms of pericarditis.

A
  1. Chest pain! Described as severe, sharp and pleuritic. Rapid onset. Pain can radiate to the arm. pleuritic
  2. Dyspnoea.
  3. Cough.
  4. Hiccups.
  5. Skin rash.
205
Q

Why might someone with pericarditis have hiccups?

A

Because of irritation to the phrenic nerve.

206
Q

What investigations might you do on someone who you suspect to have pericarditis? and what would they show?

A
  1. ECG (widespread ST elevation, PR depression)
  2. Echocardiogram (worsening pericardial effusion)
  3. Bloods (raised WBC, raised troponin)
  4. CXR (usually normal - exclude pneumonia as can cause pleural effusion)
207
Q

What might the ECG look like in someone with acute pericarditis?

A
  1. PR depression seen in most leads.

2. ‘Saddle shaped’ concave ST elevation.

208
Q

What is the major differential diagnosis of acute pericarditis?

A

MI - it is important to rule this out ASAP!

209
Q

What is the treatment for pericarditis?

A
  • Obtain blood cultures before Abx

- antimicrobials

210
Q

Why does chronic pericardial effusion rarely cause tamponade?

A

The parietal pericardium is able to adapt when effusions accumulate slowly and so tamponade is prevented.

211
Q

What is haemopericardium?

A

Direct bleeding from vasculature through the ventricular wall following MI.

212
Q

What can cause myocarditis?

A

Viral infection.

213
Q

Name 3 cardiomyopathies.

A
  1. Hypertrophic (HCM).
  2. Dilated (DCM).
  3. Arrhythmogenic right/left ventricular (ARVC/ALVC).
214
Q

What can cause HCM?

A

Sarcomeric gene mutations e.g. beta myosin, troponin T mutations. About 1 in 500 people are affected.

215
Q

What can cause ARVC/ALVC?

A

Desmosome gene mutations.

216
Q

What is the usual inheritance pattern for cardiomyopathies?

A

Autosomal dominant; off-spring have a 50% chance of being affected.

217
Q

Describe the pathophysiology of HCM.

A

Systole is normal but diastole is affected; the heart is unable to relax properly due to thickening of the ventricular walls.

218
Q

Describe the pathophysiology of DCM.

A

Ventricular dilation and dysfunction = poor contractility.

219
Q

Describe the pathophysiology of ARVC/ALVC.

A

Desmosome mutations lead to myocytes being pulled apart and ventricles are replaced with fatty fibrous tissue.

220
Q

Give 3 symptoms of HCM.

A
  1. Angina.
  2. Dyspnoea.
  3. Syncope.

think because of low CO

221
Q

Give 3 symptoms of DCM.

A

DCM usually presents with symptoms similar to those seen in heart failure:

  1. Breathlessness.
  2. Tiredness.
  3. Oedema.
222
Q

Give a sign of ARVC/ALVC.

A

Ventricular tachycardia.

223
Q

What might an ECG look like from a person with HCM.

A
  1. Large QRS complexes.

2. Large inverted T waves.

224
Q

What might an ECG look like from a person with ARVC/ALVC.

A

Epsilon waves.

225
Q

What is restrictive cardiomyopathy?

A

Poor dilation of the heart restricts diastole.

226
Q

What is the commonest cause of restrictive cardiomyopathy?

A

Amyloidosis (extra-cellular deposition of an insoluble fibrillar protein - amyloid).

227
Q

What are channelopathies?

A

Mutations in genes coding for ion channels.

228
Q

Name 2 channelopathies.

A
  1. Long QT syndrome.

2. Short QT syndrome.

229
Q

What ion channel is affected in Brugada?

A

Sodium channel.

230
Q

What is the commonest symptom of channelopathies?

A

Recurrent syncope.

231
Q

What might the ECG look like from someone with Brugada?

A

Characteristic ST elevation in chest leads.

232
Q

What is Brugada?

A

A channelopathy caused by a mutation in sodium channels.

233
Q

What are the four main features of tetralogy of fallot?

A
  1. Ventricular septal defect.
  2. Over-riding aorta.
  3. RV hypertrophy.
  4. Pulmonary stenosis.
234
Q

Would a baby born with tetralogy of fallot be cyanotic?

A

YES! There is a greater pressure in the RV than the LV and so blood is shunted into the LV -> CYANOSIS!

235
Q

What is VSD?

A

An abnormal connection between the two ventricles.

236
Q

Would a baby born with VSD be cyanotic?

A

No. There is a higher pressure in the LV than the RV and so blood is shunted from the left to right meaning there is an increased amount of blood going to the lungs; not cyanotic.

237
Q

Give 4 clinical signs of a large VSD.

A
  1. High pulmonary blood flow.
  2. Breathless, poor feeding, failure to thrive.
  3. Increased respiratory rate,
  4. Tachycardia.
  5. Requires surgical repair.
238
Q

What syndrome might VSD lead on to?

A

Eisenmengers syndrome.

239
Q

Briefly describe the physiology of Eisenmengers syndrome.

A

High pressure pulmonary blood flow damages pulmonary vasculature -> there is increased resistance to blood flow (pulmonary hypertension) -> RV pressure increases -> shunt direction reverses (RV to LV) -> CYANOSIS!

240
Q

What are the risks associated with Eisenmengers syndrome?

A
  1. Risk of death.
  2. Endocarditis.
  3. Stroke.
241
Q

What is ASD?

A

An abnormal connection between the two atria; it is fairly common.

242
Q

Would a baby born with ASD be cyanotic?

A

No. There is a higher pressure in the LA than the RA and so blood is shunted from the left to right, therefore not cyanotic.

243
Q

Give 5 clinical signs of a large ASD.

A
  1. Significant increase in blood flow through the right heart and lungs - pulmonary flow murmur.
  2. Enlarged pulmonary arteries.
  3. Right heart dilatation.
  4. Shortness of breath on exertion
  5. Increased chest infection.
244
Q

What is AVSD?

A

Atrio-ventricular septal defects. Basically a hole in the very centre of the heart.

245
Q

Give 2 clinical signs of AVSD.

A
  1. Breathless.

2. Poor feeding and poor weight gain.

246
Q

What is PDA?

which way is shunt

A

Patent ductus arteriosus.

left to right shunt => excessive pulmonary blood flow

247
Q

Give 4 clinical signs of PDA.

A
  1. Torrential flow from the aorta to the pulmonary arteries can lead to pulmonary hypertension and RHF.
  2. Breathless.
  3. Poor feeding, failure to thrive.
  4. Risk of endocarditis.
248
Q

Describe the pathophysiology behind coarctation of the aorta.

A

Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.

249
Q

What is pulmonary stenosis?

A

Narrowing of the RV outflow tract.

250
Q

Name 3 congenital heart defects that are not cyanotic.

A
  1. VSD.
  2. ASD.
  3. PDA.

Left to right shunt! This is okay but a bit insufficient and there is a risk of Eisenmengers syndrome.

251
Q

Name a congenital heart defect that is cyanotic.

A

Tetralogy of Fallot.

Right to left shunt.

252
Q

Define cardiac failure.

A

A complex clinical syndrome of signs/symptoms that suggest the efficiency of the heart as a pump is impaired; the heart is unable to deliver blood at a rate that meets the metabolic demands.

253
Q

What are the two broad categories of heart failure?

A
  1. Systolic failure: the ability of the heart to pump blood around the body is impaired.
  2. Diastolic failure: the heart is pumping blood effectively but is relaxing and filling abnormally.
254
Q

Give 5 causes of heart failure.

A
  1. Commonest cause: IHD.
  2. Hypertension.
  3. Cardiomyopathy.
  4. Excessive alcohol.
  5. Obesity.
255
Q

Why are men more commonly effected by heart failure than women?

A

Women have ‘protective hormones’ meaning they are less at risk of developing heart failure.

256
Q

Briefly describe the pathophysiology of heart failure.

A

When the heart fails, compensatory mechanisms attempt to maintain CO. As HF progresses, these mechanisms are exhausted and become pathophysiological.

257
Q

What are the compensatory mechanisms in heart failure?

A
  1. Sympathetic system.
  2. RAAS.
  3. Natriuretic peptides.
  4. Ventricular dilation.
  5. Ventricular hypertrophy.
258
Q

Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation.

A

The sympathetic system improves ventricular function by increasing HR and contractility = CO maintained.

BUT it also causes arteriolar constriction which increases after load and so myocardial work.

259
Q

Explain how RAAS is compensatory in heart failure and give one disadvantage of RAAS activation.

A

Reduced CO leads to reduced renal perfusion; this activates RAAS. There is increased fluid retention and so increased preload.

BUT it also causes arteriolar constriction which increases after load and so myocardial work.

260
Q

Give 3 properties of natriuretic peptides that make them compensatory in heart failure.

A
  1. Diuretic.
  2. Hypotensive.
  3. Vasodilators.
261
Q

What are the 3 cardinal symptoms of HF?

A
  1. Shortness of breath.
  2. Fatigue.
  3. Peripheral oedema.
262
Q

Give 3 signs of left heart failure.

A 
1. high resp rate
2 low oxygen sat
3. tachycardia
4. 3rd heart sound
5. bilateral pulmonary basal crackles (due to pulmonary oedema)
6. hypotension
263
Q

What investigations might you initially do in someone who has the signs/symptoms suggestive of HF?

A
  1. ECG.
  2. CXR - might show cardiac enlargement or pulmonary oedema
  3. Natriuretic peptide levels - raised indicate heart failure.
264
Q

You have done an ECG, CXR and blood tests on a patient who you suspect might have HF. These have come back abnormal. What investigation might you do next?

A

An echocardiogram.

265
Q

What is the first line treatment for acute LV heart failure?

A

Pour SOD

  • Pour away (stop) IV fluids
  • Sit up
  • Oxygen
  • Diuretics (IV furosemide)
266
Q

Give an example of an ACE inhibitor that is commonly used in HF.

A

Perindopril.

267
Q

Name 4 beta blockers that are used in the treatment of heart failure.

A
  1. Metoprolol.
  2. Bisoprolol.
  3. Carvedilol.
  4. Nebivolol.
268
Q

What drugs might you give to someone with HF for symptom relief.

A

Diuretics: thiazides (bendroflumethiazide) and loop diuretics (furosemide). They promote Na and so H2O excretion.

269
Q

What is cor pulmonale?

A

Right sided heart failure caused by respiratory disease.

pulmonary hypertension => RV unable to effectively pump blood to pulmonary artery => back pressure to RA => vena cava => systemic venous system

270
Q

What is the WHO clasification of hypertension?

A

140/90mmHg.

271
Q

On average, by how much does having high blood pressure shorten life?

A

7 years. Although this depends on onset and severity.

272
Q

Give 5 causes of hypertension.

A
  • primary (essential) hypertension
  • secondary: ROPE
    • Renal disease
    • Obesity
    • Pregnancy
    • Endocrine
273
Q

Name 3 endocrine diseases that can cause secondary hypertension.

A
  1. Conn’s syndrome - hyperaldosteronism.
  2. Cushing’s syndrome - prolonged cortisol exposure -> raised BP.
  3. Phaeochromocytoma - adrenal gland tumour, excess NAd and Ad release -> high BP.
274
Q

Give 3 symptoms of phaeochromocytoma?

A
  1. Pallor.
  2. Palpitations.
  3. Chest pain.
  4. Panic.
275
Q

Why might you examine the eyes of someone with hypertension?

A

Very high BP can cause immediate damage to small vessels, this can be seen in the eyes where there are small exposed blood vessle.s

276
Q

What investigations might you do in someone with hypertension?

A
  1. 24h ambulatory blood pressure monitoring to confirm a diagnosis.
  2. ECG and blood tests may be done to identify secondary causes of hypertension.
277
Q

Name 5 conditions that hypertension is a major risk factor of?

A
  1. MI (IHD).
  2. Stroke.
  3. Heart failure.
  4. Chronic renal disease.
  5. Dementia.
278
Q

If you gave someone 1 blood pressure tablet by how much would you expect their blood pressure to decrease?

A

1 tablet = 10mmHg reduction in BP.

279
Q

What is the threshold BP for giving treatment to the following:

a) high risk individuals.
b) low risk individuals.

A

a) High risk - 140/90mmHg.

b) Low risk - 160/100mmHg.

280
Q

What are the NICE treatment targets for the following:

a) People aged <80?
b) People aged >80?

A

a) Below 140/90mmHg in those aged less than 80.

b) Below 150/90mmHg in those aged above 80.

281
Q

Will anti-hypertensives make someone feel better?

A

Anti-hypertensives won’t necessarily make someone feel better as there are few symptoms associated with high BP although headache symptoms may improve.

282
Q

What are the two main types of treatment for hypertension?

A
  1. Lifestyle modification: reduce salt intake, lose weight, reduce alcohol.
  2. Drug therapy: ABCD.
283
Q

What drugs might you give to someone with hypertension?

A

A - ACEi e.g. rampiril or ARB e.g. candesartan.
B - beta blockers e.g. bisoprolol.
C - Calcium CB e.g. amlodipine, diltiazem or verapamil.
D - diuretics e.g. bendroflumethiazide or furosemide.

284
Q

Give 5 potential side effects of rampiril.

A

Side effects of ACE inhibitors:

  1. Hypotension.
  2. Acute renal failure.
  3. Hyperkalaemia.
  4. Teratogenic.
  5. Cough, rash, anaphylactoid due to increased kinin production.
285
Q

On what receptor does valsartan act?

A

AT-1, prevents Ang 2 binding.

286
Q

Give 4 side effects of valsartan.

A

Side effects of valsartan:

  1. Hypotension.
  2. Renal dysfunction.
  3. Hyperkalaemia.
  4. Rash.
  5. Contraindicated in pregnancy.
287
Q

Give 5 side effects of bisoprolol.

A

Side effects of beta blockers:

  1. Hypotension.
  2. Fatigue.
  3. Headaches.
  4. Nightmares.
  5. Bradycardia.
  6. Erectile dysfunction.
  7. Cold peripheries.
288
Q

Give 3 side effects of amlodipine.

A

Side effects of dihydropyridines (CCB):

  1. Flushing.
  2. Headache.
  3. Oedema.
  4. Palpitations.
289
Q

Give 3 side effects of verapamil.

A

Side effects due to being negatively chronotropic:
1. Bradycardia.
2. AV block.
Side effects due to being negatively inotropic:
1. Worsening of cardiac failure.

290
Q

Give 5 side effects of bendroflumethiazide.

A

Side effects of diuretics:

  1. Hypovolemia.
  2. Hypotension.
  3. Reduced K, Na, Mg, Ca.
  4. Hyperuricaemia -> gout.
  5. Erectile dysfunction.
291
Q

Name 4 valvular heart diseases.

A
  1. Aortic stenosis.
  2. Mitral regurgitation.
  3. Mitral stenosis.
  4. Aortic regurgitation.
292
Q

Briefly describe aortic stenosis.

A

A disease where the aortic orifice is restricted and so the LV can’t eject blood properly in systole = pressure overload.

293
Q

Describe the aetiology of aortic stenosis.

A
  1. Congenital bicuspid valve.

2. Acquired e.g. age related degenerative calcification and rheumatic heart disease.

294
Q

Describe the pathophysiology of aortic stenosis.

A

Aortic orifice is restricted e.g. by calcific deposits and so there is a pressure gradient between the LV and the aorta. LV function is initially maintained due to compensatory hypertrophy. Overtime this becomes exhausted = LV failure.

295
Q

Give 3 symptoms of aortic stenosis.

A
  1. Exertional syncope.
  2. Angina.
  3. Exertional sob
  4. Chest pain
  5. Fatigue
    Onset of symptoms is associated with poor prognosis.
296
Q

Give 2 signs of aortic stenosis.

A
  1. Slow rising carotid pulse and decreased pulse amplitude (murmur radiates to the carotids)
  2. Ejection systolic murmur: <> shape.
297
Q

What investigation might you do in someone who you suspect to have aortic stenosis?

A

Echocardiography.

298
Q

Describe the management for someone with aortic stenosis.

and ongoing management

A
  1. Aortic valve replacement
  2. Long term anticoagulant (warfarin)
  3. Consider IE prophylaxis
  4. Ensure good dental hygiene
299
Q

Who should be offered an aortic valve replacement?

A
  1. Symptomatic patients with aortic stenosis.
  2. Any patient with decreasing ejection fraction.
  3. Any patient undergoing CABG with moderate/severe aortic stenosis.
300
Q

What is mitral regurgitation?

A

Incompetent mitral valve allows back flow of blood from the LV to the LA during systole - LA dilatation

LV overload

301
Q

Describe the aetiology of mitral regurgitation.

A
  1. Idiopathic weakening of heart valve
  2. IHD
  3. IE
  4. Rheumatic heart disease
  5. Connective tissue diseases (Ehlers dances, marfans)
302
Q

What is the pathophysiology of mitral regurgitation?

A

LV volume overload! Compensatory mechanisms: LA enlargement and LVH and increased contractility. Progressive LV volume overload -> dilatation and progressive HF.

303
Q

Give 3 symptoms of mitral regurgitation.

A
  1. Dyspnoea on exertion.
  2. Palpitations
  3. Reduced exercise tolerance
304
Q

Give 3 signs of mitral regurgitation.

A
  1. Pansystolic high pitched whistling murmur (always there).
  2. Soft 1st heart sound.
  3. 3rd heart sound.

In chronic MR the intensity of the murmur correlates with disease severity.

305
Q

What investigations might you do in someone who you suspect to have mitral regurgitation?

A
  1. ECG (diagnostic)
  2. CXR.
  3. Echocardiogram: estimates LA/LV size and function.
306
Q

Describe the management of mitral regurgitation.

and ongoing

A
  1. if symptomatic => surgery
  2. rate control for AF (BB)
  3. anticoagulation for AF
  4. Diuretics for fluid overload
  5. IE prophylaxis
307
Q

What is aortic regurgitation?

A

A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps.

308
Q

What is the aetiology of aortic regurgitation?

A
  1. idiopathic age related weakness
  2. Rheumatic.
  3. IE.
  4. connective tissue disorders (Ehlers danlos, marfans)
309
Q

Describe the pathophysiology of aortic regurgitation.

A

Pressure and volume overload. Compensatory mechanisms - LV dilatation, LVH. Progressive dilation -> HF.

310
Q

Give 3 symptoms of aortic regurgitation.

A
  1. often asymptomatic
  2. palpitations
  3. dyspnoea on exertion
311
Q

Give 3 signs of aortic regurgitation.

A
  1. early diastolic soft murmur
  2. collapsing pulse

(H)ARD FALL => aortic regurg => Diastolic Decrescendo

312
Q

What investigations might you do in someone who you suspect to have aortic regurgitation?

A

CXR and echocardiogram.

313
Q

Describe the management for someone with aortic regurgitation.

and ongoing

A
  1. surgery (aortic valve replacement) if symptomatic
  2. Vasodilator (ACEI)
  3. IE prophylaxis
  4. regular echos
314
Q

What is mitral stenosis?

A

mitral valve narrowing => makes it hard for LA to push blood to LV

315
Q

Give 3 causes of mitral stenosis.

A
  1. Rheumatic heart disease.
  2. IE.
  3. Calcification.
316
Q

Describe the pathophysiology of mitral stenosis.

A
  • Mitral valve narrowing => increased resistance => LA hypertrophy + pulmonary congestion
  • Pulmonary venous hypertension => RHF
317
Q

Give 3 symptoms of mitral stenosis.

A
  1. Dyspnea.
  2. Haemoptysis.
  3. AF (LA strain => electrical disruption)
  4. Malar flush (back pressure of blood into pulmonary system => increased CO2 => vasodilation)
318
Q

Give 3 signs of mitral stenosis.

A
  1. ‘a’ wave in jugular venous pulsations.
  2. Signs of RHF.
  3. malar flush
  4. Low pitched diastolic rumbling murmur.
  5. Loud opening 1st heart sound snap.
319
Q

What investigations might you do in someone who you suspect to have mitral stenosis?

A
  1. ECG.
  2. CXR.
  3. Echocardiogram - gold standard.
320
Q

Describe the management for mitral stenosis.

A
  • If in AF rate control e.g. beta blockers/CCB.
  • Diuretic (furosemide)
  • Balloon valvuloplasty or valve replacement.
  • IE prophylaxis.
321
Q

Why does medication not work for mitral and aortic stenosis?

A

The problem is mechanical and so medical therapy does not prevent progression.

322
Q

What is infective endocarditis?

A

Infection of the heart valves or other endocardial lined structure within the heart.

323
Q

Name 4 types of IE.

A
  1. Left sided native IE.
  2. Left sided prosthetic IE.
  3. Right sided IE (rarely prosthetic).
  4. Device related IE e.g. pacemakers, defibrillators.
324
Q

Which type of IE is more likely to spread systemically?

A

Left sided IE - these are more likely to cause thrombo-emboli.
(Right side IE could spread to the lungs).

325
Q

Give 2 risk factors for IE.

A
  1. Having a regurgitant or prosthetic valve.
  2. If infectious material is introduced into the blood stream or during surgery.
    • IV drug users
    • Bad dental hygiene
326
Q

What bacteria are most likely to cause IE?

A

overal: s. aureus

  • Bad dental hygiene: viridian’s streptococci
  • IV drug users: Staphylococcus aureus
  • Prosthetic valves: Staph epidermis
327
Q

Give 3 groups of people who are at risk of IE.

A
  1. Elderly.
  2. IV drug users
  3. Those with prosthetic valves.
  4. Those with rheumatic fever.
328
Q

Describe the pathogenesis of IE.

A

Microbial adherence (infection) -> vegetation on valve -> cardiac valve distortion -> cardiac failure and septic problems.

329
Q

What is the hallmark of IE?

A

Vegetation - lumps of fibrin hanging off the heart valves.

330
Q

IE: Name 2 sites where vegetation is likely?

A
  1. Atrial surface of AV valves.

2. Ventricular surface of SL valves.

331
Q

Give 3 symptoms of IE.

A
  1. Signs of systemic infection e.g. fever, sweats.
  2. Embolisation e.g. stroke, PE, MI, kidney dysfunction
  3. Valve dysfunction e.g. HF, sob
332
Q

Give 5 signs of IE.

A
  1. Splinter haemorrhages.
  2. Osler’s nodes.
  3. Janeway lesions.
  4. Roth spots.
  5. Heart murmurs.
333
Q

What investigations might you do in someone who you suspect to have IE?

A
  1. Blood cultures are essential for diagnosis (before Abx)
  2. Echocardiogram (TTE or TOE)
  3. Bloods - raised ESR/CRP.
  4. ECG.
334
Q

Give 2 advantages and 1 disadvantage of a trans-thoracic echo (TTE).

A
  1. Safe.
  2. Non-invasive, no discomfort.
  3. Poor images.
335
Q

Give 1 advantage and 2 disadvantages of a trans-thoracic echo (TTE).

A
  1. Excellent images.
  2. Discomfort.
  3. Small risk of perforation or aspiration.
336
Q

Describe the treatment for IE.

A
  1. Antibiotics based on cultures.
  2. Treat any complications.
  3. Surgery.
337
Q

Give 4 indications for surgery in IE.

A
  1. Antibiotics not working.
  2. To remove infected devices.
  3. To replace the valve.
  4. to remove large vegetations before they embolise.
338
Q

Why is it important to remove large vegetations?

A

To prevent them embolising and causing a stroke, MI etc.

339
Q

Why might blood cultures be negative in a person with IE?

A

They may have previously received antibiotics.

340
Q

What is giant cell arteritis?

A

A common type of vasculitis: localised, chronic and granulomatous inflammation of temporal arteries.

341
Q

What are the signs of giant cell arteritis?

A
  1. Thickened often palpable blood vessels (temporal)

2. Evidence of granulomatous inflammation.

342
Q

Give a possible consequence of giant cell arteritis.

A

Blindness if the occular artery is affected.

343
Q

What is the name of the criteria used to diagnose IE?

A

The duke criteria.

344
Q

Name a disease might cause flattening of the P wave.

A
  1. Hyperkalaemia.

2. Obesity.

345
Q

Name a disease that might cause tall P waves.

A
  1. Right atrial enlargement.
346
Q

Name a disease that might cause broad notched P waves.

A

Left atrial enlargement.

347
Q

What aspect of the heart is represented by leads 2, 3 and aVF?

A

The inferior aspect.

348
Q

What might ST elevation in leads 2, 3 and aVF suggest?

A

RCA blockage.
These leads show the activity of the inferior aspect of the heart and the RCA supplies the inferior aspect of the heart with blood.

349
Q

Give 3 effects of hyperkalaemia on an ECG.

A
  1. Tall ‘tented’ T waves.
  2. Flat P waves.
  3. Broad QRS.
350
Q

Give 2 effects of hypokalaemia on an ECG.

A
  1. Flat T waves.
  2. QT prolongation.
  3. ST depression.
  4. Prominent U waves.
351
Q

Give an effect of hypocalcaemia on an ECG.

A
  1. QT prolongation.
  2. T wave flattening.
  3. Narrowed QRS.
  4. Prominent U waves.
352
Q

Give an effect of hypercalcaemia on an ECG.

A
  1. QT shortening.
  2. Tall T waves.
  3. No P waves.
353
Q

What is the main pacemaker in the heart?

A

The sinus node.

354
Q

What controls the sinus node discharge rate?

A

The autonomic nervous system.

355
Q

Define sinus rhythm.

A

Sinus rhythm - a P wave precedes each QRS complex.

356
Q

Give 3 potential consequences of arrhythmia.

A
  1. Sudden death.
  2. Syncope.
  3. Dizziness.
  4. Palpitations.
  5. Can also be asymptomatic.
357
Q

Define bradycardia.

A

< 60 bpm.

358
Q

Define tachycardia.

A

> 100 bpm.

359
Q

Give the two broad categories of tachycardia.

A
  1. Supra-ventricular tachycardia’s.

2. Ventricular tachycardia’s.

360
Q

Where do supra-ventricular tachycardia’s arise from?

A

They arise from the atria or atrio-ventricular junction.

361
Q

Do supra-ventricular tachycardia’s have narrow or broad QRS complexes?

A

Supraventricular tachycardias are often associated with narrow complexes.

362
Q

Where do ventricular tachycardia’s arise from?

A

The ventricles.

363
Q

Do ventricular tachycardia’s have narrow or broad QRS complexes?

A

Ventricular tachycardias are often associated with broad complexes.

364
Q

Name 5 supra-ventricular tachycardia’s.

A
  1. Atrial fibrillation.
  2. Atrial flutter.
  3. AV node re-entry tachycardia (AVNRT).
  4. Accessory pathway.
  5. Focal atrial tachycardia.
365
Q

Give 4 causes of sinus tachycardia.

A
  1. Physiological response to exercise.
  2. Fever,
  3. Anaemia.
  4. Heart failure.
  5. Hypovolemia.
366
Q

Describe 2 characteristics of an ECG taken from someone with atrial fibrillation.

A
  1. Absent P waves.

2. Fine oscillation of the baseline.

367
Q

The ECG taken from someone with atrial fibrillation shows a fine oscillation of the baseline and absent P waves. Why?

A

The atria fire a lot, it is chaotic. The AV node and ventricles can’t keep up -> irregularly irregular pulse.

368
Q

Give 4 symptoms of atrial fibrillation.

A
  1. Palpitations.
  2. Shortness of breath.
  3. Fatigue.
  4. Chest pain.
  5. Increased risk of thromboembolism and therefore stroke.
369
Q

What score can be used to calculate the risk of stroke in someone with atrial fibrillation?

A

CHADS2 VASc.

370
Q

What does the CHADS2 VASc score take into account?

A

The CHADS2 VASc score is used to calculate the risk of stroke in patients with atrial fibrillation. It considers:

  1. Age.
  2. Hypertension.
  3. Previous stroke/TIA.
  4. Diabetes.
  5. Female.

A score >2 indicates the need for anticoagulation.

371
Q

Describe the treatment for atrial fibrillation.

A
  1. Rate control - BB (bisopralol), CCB (diltiazem) and digoxin.
  2. Rhythm control - electrical cardioversion or pharmacological cardioversion (amiodarone)
  3. ongoing DOAC (apixiban)
372
Q

Atrial fibrillation treatment: what might you give someone to help with rate control?

A

Beta blockers (bisoprolol), CCB (diltiazem, verapamil) and digoxin.

373
Q

Atrial fibrillation treatment: what might you give someone to help restore sinus rhythm (rhythm control)?

A

Electrical cardioversion or pharmacological cardioversion (flecainide or amiodarone)

374
Q

What is the long term treatment of atrial fibrillation?

A

anticoagulation: DOAC - apixiban

rate control: BB - bisoprolol

375
Q

Describe the ECG pattern taken from someone with atrial flutter.

A
  1. Narrow QRS.

2. ‘sawtooth’ flutter waves.

376
Q

The ECG shows a continuous undulating pattern and sawtooth flutter waves. What arrhythmia is this describing?

A

Atrial flutter.

377
Q

What pathophysiological mechanism can cause atrial flutter?

A

The re-entry mechanism - there is blockage of the normal circuit. Another pathway forms, takes a different course and re-enters the circuit -> tachycardia.

378
Q

What is the commonest supra-ventricular tachycardia?

A

AV node re-entry tachycardia (AVNRT).

379
Q

Do you see P waves in AVNRT?

A

No - the P waves are within the QRS complex.

380
Q

Give 4 symptoms of AVNRT.

A
  1. Sudden onset/offset palpitations.
  2. Neck pulsation.
  3. Chest pain.
  4. Shortness of breath.
381
Q

Describe the acute treatment of AVNRT.

A

Acute treatment: vagal manoeuvre and adenosine.

382
Q

What drugs might you give to someone to suppress future episodes of AVNRT?

A

Beta blockers, CCB, flecainide.

383
Q

Describe the pathophysiology of accessory pathway arrhythmias.

A

Congenital muscle strands connect the atria and ventricles - accessory pathway. This can result in pre-excitation of ventricles.

384
Q

Describe 3 characteristics of an ECG taken from someone with accessory pathway arrhythmia.

A
  1. Delta wave.
  2. Short PR interval.
  3. Slurred QRS complex.
385
Q

Give an example of an accessory pathway arrhythmia.

A

Wolff-Parkinson-White syndrome.

386
Q

Describe the pathophysiology of focal atrial tachycardia.

A

Another area of the atrium becomes more autonomic than the sinus node and so sinus node function is taken over -> focal atrial tachycardia.

387
Q

What might you see on an ECG taken from someone with focal atrial tachycardia.

A

Abnormal P waves appear before a normal QRS.

388
Q

What is the treatment for ventricular tachycardia in an urgent situation?

A

DC cardioversion.

389
Q

What is the long term treatment for ventricular tachycardia in high risk patients?

A

Implantable defibrillator.

390
Q

What are ectopic beats?

A

Very common, generally benign arrhythmias caused by premature discharge. The patient may complain of symptoms of ‘skipped beats’.

391
Q

Give 3 causes of long QT syndrome.

A
  1. Congenital.
  2. Electrolyte disturbances e.g. hypokalaemia and hypocalcaemia.
  3. A variety of drugs (amiodarone, stall, flecanide)
392
Q

Give 2 signs of long QT syndrome.

A
  1. Palpitations.

2. Syncope.

393
Q

Give 4 causes of sinus bradycardia.

A
  1. Ischaemia.
  2. Fibrosis of the atrium.
  3. Inflammation.
  4. Drugs.
394
Q

Give 3 causes of heart block.

A
  1. CAD.
  2. Cardiomyopathy.
  3. Fibrosis.
395
Q

What kind of heart block is associated with wide QRS complexes with an abnormal pattern?

A

RBBB or LBBB.

396
Q

Describe first degree AV block.

A

Fixed prolongation of the PR interval due to delayed conduction to the ventricles.

397
Q

Describe second degree AV block.

A

There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles and so you don’t get a QRS complex.

398
Q

Types of second degree AV block: describe Mobitz type 1.

A

PR interval gradually increases until AV node fails and no QRS is seen. (ill be back)

399
Q

Types of second degree AV block: describe Mobitz type 2.

A

There is a sudden unpredictable loss of AV conduction and so loss of QRS. PR interval is constant but every nth QRS complex is missing.

400
Q

Describe third degree AV block.

A

Atrial activity fails to conduct to the ventricles. P waves and QRS complexes therefore occur independently.

401
Q

LBBB: what would you see in lead V1 and V6?

A

A ‘W’ shape would be seen in the QRS complex of lead V1 and a ‘M’ shape in V6.

WiLLiaM.

402
Q

RBBB: what would you see in lead V1 and V6?

A

A ‘M’ shape would be seen in the QRS complex of lead V1 and a ‘W’ shape in V6.

MaRRoW.

403
Q

Cardiac arrhythmias: what is the treatment of choice in a patient who is hemodynamically unstable due to the underlying rhythm?

A

DC cardioversion.

404
Q

What is a consequence of peripheral arterial occlusion?

A

Gangrene.

405
Q

Give 2 diseases that result from stress indicued ischaemia.

A
  1. Exercise induced angina.

2. Intermittent claudication.

406
Q

Give 2 diseases that result from ischaemia due to structural/functional breakdown.

A
  1. Critical limb ischaemia.

2. Vascular dementia.

407
Q

Give a sign of infarction.

A

Gangrene.

408
Q

What is intermittent claudication?

A

A symptom describing muscle pain that is caused by moderate ischaemia. Intermittent claudication occurs when exercising (stress induced) and is relieved with rest.

409
Q

What can intermittent claudication lead on to if left untreated?

A

Critical ischaemia.

410
Q

Intermittent claudication: is O2 supply normal or low at rest and when you begin exercise?

A

Normal. Intermittent claudication is stress induced so at rest and when you begin exercise O2 supply is able to meet demand.

411
Q

Intermittent claudication: is O2 supply normal or low when you do moderate/hard exercise?

A

Low. O2 supply is unable to meet demand -> anaerobic respiration -> lactic acid.

412
Q

Intermittent claudication: is O2 supply normal or low after a short rest?

A

Low. It takes longer to recover as you’re getting rid of the lactic acid. After a long rest however it is normal.

413
Q

Give a symptom of intermittent claudication.

A

Muscle cramps.

414
Q

What is critical ischaemia?

A

Blood supply is barely adequate for life. There is no reserve for an increase in demand. Very severe, cells are dying.
O2 supply is ALWAYS low, even at rest!

415
Q

Give 4 signs of critical ischaemia.

A
  1. Rest pain.
  2. Classically nocturnal.
  3. Ulceration.
  4. Gangrene.
416
Q

What can cause acute ischaemia?

A

Embolism/thrombosis.

417
Q

Give 6 symptoms of acute ischaemia.

A

6P

  1. Pain.
  2. Pale.
  3. Paralysis.
  4. Paraesthesia.
  5. Perishing cold.
  6. Pulseless.
418
Q

Give 2 examples of acute ischaemia.

A
  1. Stroke.

2. MI.

419
Q

Give 5 risk factors for peripheral vascular disease.

A
  1. Hypertension.
  2. Hyperlipidaemia.
  3. Diabetes.
  4. Smoking.
  5. Obesity.
420
Q

Give 4 treatments for peripheral vascular disease.

A
  1. Risk factor modification.
  2. Vein bypass for critical leg ischaemia.
  3. Balloon angioplasty.
  4. Stenting of occlusion.
  5. Amuptation.
421
Q

Describe 4 steps in the initial management of a STEMI.

A
  1. ABCDE.
  2. Morphine.
  3. Oxygen (if hypoxic).
  4. Nitrates.
  5. Aspirin.
422
Q

PCI is the treatment of choice for a STEMI. What might you do instead if you were unable to do PCI?

A

Thrombolysis using streptokinase.

423
Q

Name a drug that can be used for thrombolysis in the treatment of a STEMI.

A

Streptokinase.

424
Q

In what type of valvular heart disease would you hear a mid-diastolic murmur and a 1st heart sound snap?

A

Mitral stenosis.

425
Q

In what type of valvular heart disease would you hear a pan-systolic murmur?

A

Mitral regurgitation.

426
Q

In what type of valvular heart disease would you hear a ejection systolic murmur?

A

Aortic stenosis.

427
Q

In what type of valvular heart disease would you see a wide pulse pressure and hear an early diastolic blowing murmur and systolic ejection murmur?

A

Aortic regurgitation.

428
Q

Name the criteria that is used in the diagnosis of infective endocarditis.

A

Duke’s criteria.

429
Q

Give 2 major points in the Duke’s criteria that if present can confirm a diagnosis of IE.

A
  1. Positive blood culture with typical IE microorganism.

2. Positive echo showing endocardial involvement.

430
Q

What organism can cause rheumatic fever?

A

Group A strep e.g. s.pyogenes.

431
Q

A lady presents with a tearing pain and is found to have hypertension. A CT scan is done and a ‘tennis ball sign’ is observed. What is the likely pathology behind the patient’s pain?

A

Aortic dissection!

432
Q

What type of drug is digoxin?

A

Digoxin is a cardiac glycoside.

433
Q

What is a typical lesion of atherosclerosis?

A

Fatty streaks.

434
Q

Write an equation for mAP.

A

mAP = DP + 1/3 PP.

435
Q

What is the cause of reactive hyperaemia?

A

When blood flow increases following occlusion to arterial flow.

436
Q

Give the equation for BP.

A

BP = CO x TPR.

437
Q

Give the equation for stroke volume.

A

SV = EDV - ESV.

438
Q

Give the equation for cardiac output.

A

CO = SV x HR.

439
Q

Name the classification system for peripheral vascular disease (PVD).

A

Fontaine classification.

440
Q

Why does mitral stenosis cause AF?

A

There is increased LA pressure. This stretches the myocytes in the atria and irritates pacemaker cells -> AF.

441
Q

Why does mitral stenosis lead to a raised JVP?

A

Pulmonary congestion -> pulmonary hypertension causes a raised JVP.

442
Q

Why might someone with mitral stenosis be breathless? Use Sterling’s law in your explanation.

A

Mitral stenosis means ventricles don’t fill completely -> reduced EDV -> reduced SV -> reduced CO and so breathlessness.

443
Q

Give 2 ECG signs of PE.

A
  1. Sinus tachycardia.

2. Atrial fibrillation.

444
Q

Name 2 diseases that are due to moderate ischaemia.

A
  1. Angina.

2. Intermittent claudication.

445
Q

Name a disease that is due to severe ischaemia.

A

Critical limb ischaemia.

446
Q

Give 2 signs of RHF.

A
  1. Raised JVP.

2. Ascites.

447
Q

Describe the NYHA classification for heart failure.

A
  1. Class 1: heart disease is present but there is no limitation.
  2. Class 2: comfortable at rest but slight limitation on activity - mild HF.
  3. Class 3: marked limitation - moderate HF.
  4. Class 4: SOB at rest, all activity causes discomfort (moderate HF).
448
Q

Give 4 signs you might see on a CXR taken from someone with heart failure.

A
  1. Pleural effusion.
  2. Dilated pulmonary arteries.
  3. Kerley B lines.
  4. Bat’s wings.
  5. Cardiomegaly.
449
Q

What coronary event might Dressler’s syndrome develop after?

A

(pericarditis) Can develop 2-10 weeks after an MI

.

450
Q

What is Dressler’s syndrome?

A

Myocardial injury stimulates formation of autoantibodies against the heart. Cardiac tamponade may occur. Dressler’s is a secondary form of pericarditis.

451
Q

Give 3 symptoms of Dressler’s syndrome.

A
  1. Fever.
  2. Chest pain.
  3. Pericardial rub.

Occurs 2-10 week after MI.

452
Q

Describe the treatment for an MI.

A
  1. MONA.
  2. PCI or streptokinase.

ongoing: Aspirin, Another anti platelet (clopigodrel), atorvastatin, ACEi (ramipril), atenolol (or other BB), Aldosterone antagonist (if HF)

453
Q

How does LMWH work?

A

It activates anti-thrombin, which then inhibits thrombin and factor 10a.

454
Q

Define ischaemia.

A

Reversible tissue damage as a result of impaired vascular perfusion depriving tissues of nutrients and oxygen.

455
Q

Define infarction.

A

Irreversible tissue death due to ischaemia.

456
Q

Why might someone with HF feel tired?

A

Due to reduced CO.

457
Q

Why might someone with HF feel breathless when lying down?

A

Due to pulmonary oedema.

458
Q

Why might someone with HF have tachycardia?

A

Due to activation of the sympathetic system.

459
Q

Why might someone with HF have peripheral oedema?

A
  1. Decreased venous pressure.

2. RAAS activation -> sodium and H2O retention.

460
Q

Give 3 clinical features of shock.

A
  1. Low blood pressure.
  2. Rapid pulse.
  3. Low urine output.
  4. Pallor.
  5. Sweating.
461
Q

Give 5 signs of anaphylactic shock.

A
  1. Breathlessness.
  2. Wheeze.
  3. Rash.
  4. Swollen lips/tongue.
  5. Low BP.
  6. Chest tightness.
462
Q

Why might someone with anaphylactic shock have a low BP?

A
  1. Vasodilation.

2. Increased vascular permeability.

463
Q

State two common allergens responsible for causing anaphylactic shock.

A
  1. Seafood.
  2. Nuts.
  3. Grains.

2a (12 decks)

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